This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. This project is intended to increase understanding of development though examination of the molecular/genetic mechanism by which the hormone auxin (indole acetic acid) directs leaf expansion in the model plant Arabidopsis thaliana. Auxin is known to trigger selective degradation of transcription factors via the ubiqutin-26S proteosome pathway. It is not known, however, how hormone reception leads to accelerated transcription factor degradation and altered developmental physiology although earlier work in this laboratory suggests auxin interacts, in advance of transcription factor proteolysis, with a second non-auxin growth effecter in controlling leaf expansion. We will use mutational analysis to address the specific aims proposed here which include (1) identifing the gene(s) associated with production of the hypothesized growth effector and (2) identifying genes responsible for other signal transduction players in auxin control of leaf expansion in plants. Understanding of the regulation of ubiquitination in plants may provide insights into the function of the orthologous human system. Several human cancers result from ubiquitin pathway malfunction. Auxins are also suspected endocrine disrupters. The results of this subproject may also lead to an understanding of how these compounds function in disturbing mammalian development. Since the start date of this sub-project, January 1, 2005, a large reach-in growth chamber (AC-60 "Bigfoot";Enconair, Winnipeg, Canada), essential for establishing uniform conditions underwhich to grow and screen mutated plants, has been purchased and installed. A series of preliminary growth experiments have been initiated to optimize growth conditions. A large number of wild type Arabidopsis seeds (CS 1092;Lehle Seeds, Round Rock, TX) have been mutagenized with ethyl methane sulfonate at a range of concentrations. Mutated seed (M1) has been grown for seed (M2). The cells of the M2 are expected to contain homozygous mutations which will be screened for phenotypes of interest.